Abstracts must be submitted as an MS WORD document only.
All abstracts must meet formatting requirements (see sample). Abstracts that do not meet all formatting/submission guidelines will not be accepted.
Abstracts must not exceed 250 words, excluding title, authors, and institutions.
Abstracts should be typed, single space in Times New Roman, 11 point font.
Abstract title must be bold and typed in ALL CAPITAL LETTERS.
Authors should be listed as follows:
*Joan A. Doe, Thomas T. Smith, and Carl Jones
More than one student presenter is allowed for poster presentations. Only one presenter is allowed for oral presentations. (*Indicates the student presenter).
List Department, Institution, City, State, Zip Code as follows:
Department of Biology, Morgan State University, Baltimore, MD 21251.
Skip one line, indent (5) spaces, and begin typing the abstract.
Abstracts should contain the following:
1. INTRODUCTION outlining the significance of the research project. (For the arts categories, the introduction should state the problem/nature and significance of the topic.)
2. Statement of the HYPOTHESIS being tested or the OBJECTIVE for the research.
3. Brief statement of RESEARCH METHODS used. (For the arts, state the method/investigative strategy.)
4. Summary of the RESULTS.
5. Statement of the CONCLUSIONS.
6. A list of grants that support your abstract.
IDENTIFICATION OF GAMMA-2-MELANOCYTE STIMULATING HORMONE (ɣ-2-MSH) RESPONSIVE GENES IN MC3R TRANSFECTED BRAINSTEM CAD CELLS BY MICROARRAY ANALYSIS. *Segun Bernard, Brian Redmond, James Wachira and Cleo Hughes Darden. Morgan State University, Department of Biology, Baltimore, MD 21251.
Melanocortins are peptide hormones that are derived from the precursor polypeptide pro-opiomelanocortin. They mediate their effects through a family) of five G-protein coupled receptors, the melanocortin receptors. Some studies have implicated other signaling pathways such as the PKC, MAP kinase, and the JAK/STAT pathways. Melanocortin receptors, melanocortin-3-receptor (MC3R) and melanocortin-4-receptor (MC4R), have been implicated in the pathophysiology of obesity, insulin resistance and salt-sensitive hypertension through gene knockout studies. In order to understand the molecular mechanisms involved in MC3R signaling, we treated MC3R/GFP and GFP control transfected cells with gamma-MSH and isolated total RNA for gene transcription analysis using oligonucleotide microarrays. Total RNA isolated from the two populations of harvested cells was amplified, labeled and co-hybridized to oligonucleotide microarrays. Eighty-eight genes were up-regulated and 91 genes were down-regulated with > 2 ratio and p-value of < 0.05. Several pathways were altered including signal transduction and G-protein coupled receptor protein signaling, among others. Quantitative PCR data indicate that protein tyrosine phosphatase and protein kinase nu genes are up-regulated as a result of MC3R activation by gamma-MSH. The information gathered from this study will enhance our knowledge of the molecular mechanisms involved in MC3R signaling because of its involvement in salt sensitive hypertension and cardiovascular function. (Supported by NIH/NCRR/RCMI/G12RR17581-05 and RCMI funded core facilities)